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<p><small><strong>Figure 1. RNA immunoprecipitation using the Diagenode monoclonal antibody directed against psU</strong><br />RNA immunoprecipitation (RIP) was performed on 40 µg total RNA isolated from HeLa cells using 5 µg of the Diagenode monoclonal antibody against psU (Cat. No. C15200247) or with an equal amount of mouse IgG, used as a negative control. The immunoprecipitated RNA was subsequently analysed on a Bioanalyzer. Figure 1A shows the Bioanalyzer profile obtained with the psU antibody (right) The left panel shows the input. Figure 1B shows the gel image for the psU antibody, the IgG negative control and the input (lane 1, 2 and 3, respectively). The marker (in bp) is shown on the left, the position of the 28s and 18s ribosomal RNA is indicated on the right.</small></p>
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<p><small><strong>Figure 2. RIP using the Diagenode monoclonal antibody directed against psU</strong><br />RIP assays were performed on 40 µg total RNA from human HeLa cells using the Diagenode antibody against psU (Cat. No. C15200247). A titration of the antibody consisting of 1, 2 and 5 µg per RIP experiment was analysed. IgG (2 µg/IP) was used as negative IP control. QRT-PCR was performed with primers for the 18 and 28s rRNA genes, for the RPL19 and ATP5E mRNA, shown to contain a psU residue and for the MB gene, used as a negative control. Figure 2 shows the recovery, expressed as a % of input (the relative amount of immunoprecipitated DNA compared to input DNA after qPCR analysis).</small></p>
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<p><small><strong>Figure 1. RNA immunoprecipitation using the Diagenode monoclonal antibody directed against psU</strong><br />RNA immunoprecipitation (RIP) was performed on 40 µg total RNA isolated from HeLa cells using 5 µg of the Diagenode monoclonal antibody against psU (Cat. No. C15200247) or with an equal amount of mouse IgG, used as a negative control. The immunoprecipitated RNA was subsequently analysed on a Bioanalyzer. Figure 1A shows the Bioanalyzer profile obtained with the psU antibody (right) The left panel shows the input. Figure 1B shows the gel image for the psU antibody, the IgG negative control and the input (lane 1, 2 and 3, respectively). The marker (in bp) is shown on the left, the position of the 28s and 18s ribosomal RNA is indicated on the right.</small></p>
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<p><small><strong>Figure 2. RIP using the Diagenode monoclonal antibody directed against psU</strong><br />RIP assays were performed on 40 µg total RNA from human HeLa cells using the Diagenode antibody against psU (Cat. No. C15200247). A titration of the antibody consisting of 1, 2 and 5 µg per RIP experiment was analysed. IgG (2 µg/IP) was used as negative IP control. QRT-PCR was performed with primers for the 18 and 28s rRNA genes, for the RPL19 and ATP5E mRNA, shown to contain a psU residue and for the MB gene, used as a negative control. Figure 2 shows the recovery, expressed as a % of input (the relative amount of immunoprecipitated DNA compared to input DNA after qPCR analysis).</small></p>
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<p><small><strong>Figure 1. RNA immunoprecipitation using the Diagenode monoclonal antibody directed against psU</strong><br />RNA immunoprecipitation (RIP) was performed on 40 µg total RNA isolated from HeLa cells using 5 µg of the Diagenode monoclonal antibody against psU (Cat. No. C15200247) or with an equal amount of mouse IgG, used as a negative control. The immunoprecipitated RNA was subsequently analysed on a Bioanalyzer. Figure 1A shows the Bioanalyzer profile obtained with the psU antibody (right) The left panel shows the input. Figure 1B shows the gel image for the psU antibody, the IgG negative control and the input (lane 1, 2 and 3, respectively). The marker (in bp) is shown on the left, the position of the 28s and 18s ribosomal RNA is indicated on the right.</small></p>
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<p><small><strong>Figure 2. RIP using the Diagenode monoclonal antibody directed against psU</strong><br />RIP assays were performed on 40 µg total RNA from human HeLa cells using the Diagenode antibody against psU (Cat. No. C15200247). A titration of the antibody consisting of 1, 2 and 5 µg per RIP experiment was analysed. IgG (2 µg/IP) was used as negative IP control. QRT-PCR was performed with primers for the 18 and 28s rRNA genes, for the RPL19 and ATP5E mRNA, shown to contain a psU residue and for the MB gene, used as a negative control. Figure 2 shows the recovery, expressed as a % of input (the relative amount of immunoprecipitated DNA compared to input DNA after qPCR analysis).</small></p>
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<li>Highly sensitive and specific</li>
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'description' => '<h3 class="c-article__sub-heading" data-test="abstract-sub-heading">Background</h3>
<p>Previous studies have indicated that ψ-modified small RNAs play crucial roles in tumor metastasis. However, the ψ-modified small RNAs during metastasis of PTC are still unclear.</p>
<h3 class="c-article__sub-heading" data-test="abstract-sub-heading">Methods</h3>
<p>We compared the pseudouridine synthase 7 (PUS7) alteration between metastatic and non-metastatic PTCs, and investigated its correlation with clinicopathological features. Additionally, we employed a small RNA ψ modification microarray to examine the small RNA ψ modification profile in both metastatic and non-metastatic PTCs, as well as paired paracancerous tissues. The key molecule involved in ψ modification, pre-miR-8082, was identified and found to regulate the expression of CD47. Experiments in vitro were conducted to further investigate the function of PUS7 and CD47 in PTC.</p>
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<p>Our results demonstrated that PUS7 was down-regulated in PTC and was closely associated with metastasis. Moreover, the ψ modification of pre-miR-8082 was found to be decreased, resulting in down-expression of pre-miR-8082 and miR-8082, leading to the loss of the inhibitory effect on CD47, thereby promoting tumor migration.</p>
<h3 class="c-article__sub-heading" data-test="abstract-sub-heading">Conclusions</h3>
<p>Our study demonstrates that PUS7 promotes the inhibition of CD47 and inhibits metastasis of PTC cells by regulating the ψ modification of pre-miR-8082. These results suggest that PUS7 and ψ pre-miR-8082 may serve as potential targets and diagnostic markers for PTC metastasis.</p>',
'date' => '2024-10-14',
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<p>Previous studies have indicated that ψ-modified small RNAs play crucial roles in tumor metastasis. However, the ψ-modified small RNAs during metastasis of PTC are still unclear.</p>
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<p>We compared the pseudouridine synthase 7 (PUS7) alteration between metastatic and non-metastatic PTCs, and investigated its correlation with clinicopathological features. Additionally, we employed a small RNA ψ modification microarray to examine the small RNA ψ modification profile in both metastatic and non-metastatic PTCs, as well as paired paracancerous tissues. The key molecule involved in ψ modification, pre-miR-8082, was identified and found to regulate the expression of CD47. Experiments in vitro were conducted to further investigate the function of PUS7 and CD47 in PTC.</p>
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<p>Our results demonstrated that PUS7 was down-regulated in PTC and was closely associated with metastasis. Moreover, the ψ modification of pre-miR-8082 was found to be decreased, resulting in down-expression of pre-miR-8082 and miR-8082, leading to the loss of the inhibitory effect on CD47, thereby promoting tumor migration.</p>
<h3 class="c-article__sub-heading" data-test="abstract-sub-heading">Conclusions</h3>
<p>Our study demonstrates that PUS7 promotes the inhibition of CD47 and inhibits metastasis of PTC cells by regulating the ψ modification of pre-miR-8082. These results suggest that PUS7 and ψ pre-miR-8082 may serve as potential targets and diagnostic markers for PTC metastasis.</p>',
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<p><small><strong>Figure 1. RNA immunoprecipitation using the Diagenode monoclonal antibody directed against psU</strong><br />RNA immunoprecipitation (RIP) was performed on 40 µg total RNA isolated from HeLa cells using 5 µg of the Diagenode monoclonal antibody against psU (Cat. No. C15200247) or with an equal amount of mouse IgG, used as a negative control. The immunoprecipitated RNA was subsequently analysed on a Bioanalyzer. Figure 1A shows the Bioanalyzer profile obtained with the psU antibody (right) The left panel shows the input. Figure 1B shows the gel image for the psU antibody, the IgG negative control and the input (lane 1, 2 and 3, respectively). The marker (in bp) is shown on the left, the position of the 28s and 18s ribosomal RNA is indicated on the right.</small></p>
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<p><small><strong>Figure 2. RIP using the Diagenode monoclonal antibody directed against psU</strong><br />RIP assays were performed on 40 µg total RNA from human HeLa cells using the Diagenode antibody against psU (Cat. No. C15200247). A titration of the antibody consisting of 1, 2 and 5 µg per RIP experiment was analysed. IgG (2 µg/IP) was used as negative IP control. QRT-PCR was performed with primers for the 18 and 28s rRNA genes, for the RPL19 and ATP5E mRNA, shown to contain a psU residue and for the MB gene, used as a negative control. Figure 2 shows the recovery, expressed as a % of input (the relative amount of immunoprecipitated DNA compared to input DNA after qPCR analysis).</small></p>
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<p><small><strong>Figure 1. RNA immunoprecipitation using the Diagenode monoclonal antibody directed against psU</strong><br />RNA immunoprecipitation (RIP) was performed on 40 µg total RNA isolated from HeLa cells using 5 µg of the Diagenode monoclonal antibody against psU (Cat. No. C15200247) or with an equal amount of mouse IgG, used as a negative control. The immunoprecipitated RNA was subsequently analysed on a Bioanalyzer. Figure 1A shows the Bioanalyzer profile obtained with the psU antibody (right) The left panel shows the input. Figure 1B shows the gel image for the psU antibody, the IgG negative control and the input (lane 1, 2 and 3, respectively). The marker (in bp) is shown on the left, the position of the 28s and 18s ribosomal RNA is indicated on the right.</small></p>
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<p><small><strong>Figure 2. RIP using the Diagenode monoclonal antibody directed against psU</strong><br />RIP assays were performed on 40 µg total RNA from human HeLa cells using the Diagenode antibody against psU (Cat. No. C15200247). A titration of the antibody consisting of 1, 2 and 5 µg per RIP experiment was analysed. IgG (2 µg/IP) was used as negative IP control. QRT-PCR was performed with primers for the 18 and 28s rRNA genes, for the RPL19 and ATP5E mRNA, shown to contain a psU residue and for the MB gene, used as a negative control. Figure 2 shows the recovery, expressed as a % of input (the relative amount of immunoprecipitated DNA compared to input DNA after qPCR analysis).</small></p>
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<p>Previous studies have indicated that ψ-modified small RNAs play crucial roles in tumor metastasis. However, the ψ-modified small RNAs during metastasis of PTC are still unclear.</p>
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<p>Previous studies have indicated that ψ-modified small RNAs play crucial roles in tumor metastasis. However, the ψ-modified small RNAs during metastasis of PTC are still unclear.</p>
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<p>We compared the pseudouridine synthase 7 (PUS7) alteration between metastatic and non-metastatic PTCs, and investigated its correlation with clinicopathological features. Additionally, we employed a small RNA ψ modification microarray to examine the small RNA ψ modification profile in both metastatic and non-metastatic PTCs, as well as paired paracancerous tissues. The key molecule involved in ψ modification, pre-miR-8082, was identified and found to regulate the expression of CD47. Experiments in vitro were conducted to further investigate the function of PUS7 and CD47 in PTC.</p>
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<p>Our results demonstrated that PUS7 was down-regulated in PTC and was closely associated with metastasis. Moreover, the ψ modification of pre-miR-8082 was found to be decreased, resulting in down-expression of pre-miR-8082 and miR-8082, leading to the loss of the inhibitory effect on CD47, thereby promoting tumor migration.</p>
<h3 class="c-article__sub-heading" data-test="abstract-sub-heading">Conclusions</h3>
<p>Our study demonstrates that PUS7 promotes the inhibition of CD47 and inhibits metastasis of PTC cells by regulating the ψ modification of pre-miR-8082. These results suggest that PUS7 and ψ pre-miR-8082 may serve as potential targets and diagnostic markers for PTC metastasis.</p>',
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<p>Previous studies have indicated that ψ-modified small RNAs play crucial roles in tumor metastasis. However, the ψ-modified small RNAs during metastasis of PTC are still unclear.</p>
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<p>Our results demonstrated that PUS7 was down-regulated in PTC and was closely associated with metastasis. Moreover, the ψ modification of pre-miR-8082 was found to be decreased, resulting in down-expression of pre-miR-8082 and miR-8082, leading to the loss of the inhibitory effect on CD47, thereby promoting tumor migration.</p>
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<p>Our study demonstrates that PUS7 promotes the inhibition of CD47 and inhibits metastasis of PTC cells by regulating the ψ modification of pre-miR-8082. These results suggest that PUS7 and ψ pre-miR-8082 may serve as potential targets and diagnostic markers for PTC metastasis.</p>',
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<p>Previous studies have indicated that ψ-modified small RNAs play crucial roles in tumor metastasis. However, the ψ-modified small RNAs during metastasis of PTC are still unclear.</p>
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<p>Our study demonstrates that PUS7 promotes the inhibition of CD47 and inhibits metastasis of PTC cells by regulating the ψ modification of pre-miR-8082. These results suggest that PUS7 and ψ pre-miR-8082 may serve as potential targets and diagnostic markers for PTC metastasis.</p>',
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'name' => 'Pseudouridine Monoclonal Antibody datasheet',
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'name' => 'Dysregulation of pseudouridylation in small RNAs contributes to papillary thyroid carcinoma metastasis',
'authors' => 'Xi Wang et al.',
'description' => '<h3 class="c-article__sub-heading" data-test="abstract-sub-heading">Background</h3>
<p>Previous studies have indicated that ψ-modified small RNAs play crucial roles in tumor metastasis. However, the ψ-modified small RNAs during metastasis of PTC are still unclear.</p>
<h3 class="c-article__sub-heading" data-test="abstract-sub-heading">Methods</h3>
<p>We compared the pseudouridine synthase 7 (PUS7) alteration between metastatic and non-metastatic PTCs, and investigated its correlation with clinicopathological features. Additionally, we employed a small RNA ψ modification microarray to examine the small RNA ψ modification profile in both metastatic and non-metastatic PTCs, as well as paired paracancerous tissues. The key molecule involved in ψ modification, pre-miR-8082, was identified and found to regulate the expression of CD47. Experiments in vitro were conducted to further investigate the function of PUS7 and CD47 in PTC.</p>
<h3 class="c-article__sub-heading" data-test="abstract-sub-heading">Results</h3>
<p>Our results demonstrated that PUS7 was down-regulated in PTC and was closely associated with metastasis. Moreover, the ψ modification of pre-miR-8082 was found to be decreased, resulting in down-expression of pre-miR-8082 and miR-8082, leading to the loss of the inhibitory effect on CD47, thereby promoting tumor migration.</p>
<h3 class="c-article__sub-heading" data-test="abstract-sub-heading">Conclusions</h3>
<p>Our study demonstrates that PUS7 promotes the inhibition of CD47 and inhibits metastasis of PTC cells by regulating the ψ modification of pre-miR-8082. These results suggest that PUS7 and ψ pre-miR-8082 may serve as potential targets and diagnostic markers for PTC metastasis.</p>',
'date' => '2024-10-14',
'pmid' => 'https://link.springer.com/article/10.1186/s12935-024-03482-3',
'doi' => 'https://doi.org/10.1186/s12935-024-03482-3',
'modified' => '2024-10-18 11:41:05',
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$externalLink = ' <a href="https://link.springer.com/article/10.1186/s12935-024-03482-3" target="_blank"><i class="fa fa-external-link"></i></a>'include - APP/View/Products/view.ctp, line 755
View::_evaluate() - CORE/Cake/View/View.php, line 971
View::_render() - CORE/Cake/View/View.php, line 933
View::render() - CORE/Cake/View/View.php, line 473
Controller::render() - CORE/Cake/Controller/Controller.php, line 963
ProductsController::slug() - APP/Controller/ProductsController.php, line 1052
ReflectionMethod::invokeArgs() - [internal], line ??
Controller::invokeAction() - CORE/Cake/Controller/Controller.php, line 491
Dispatcher::_invoke() - CORE/Cake/Routing/Dispatcher.php, line 193
Dispatcher::dispatch() - CORE/Cake/Routing/Dispatcher.php, line 167
[main] - APP/webroot/index.php, line 118
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